Question 1

Humanized anti-IL-2 receptor therapy — Preliminary clinical results with a humanized antibody against the IL-2 receptor suggested which outcome regarding HAMA (human anti-mouse antibody) responses and recognition of Ig constant regions?

Accepted Answer

Introduction / Context: Fully murine monoclonal antibodies often elicit HAMA responses, reducing efficacy and safety. Humanization reduces murine sequences in the variable regions while retaining antigen specificity, aiming to diminish immunogenicity and extend therapeutic utility (e.g., anti-IL-2R antibodies for immune modulation). Given Data / Assumptions: Humanized antibodies are predominantly human in framework and constant regions. Reduced murine content should lower anti-mouse immune responses (HAMA). Clinical endpoints include safety, immunogenicity, and pharmacokinetics. Concept / Approach: The logical prediction—and what early trials supported—is that humanized anti-IL-2R antibodies show reduced HAMA compared with murine counterparts, improving tolerability and enabling repeated dosing without rapid clearance or hypersensitivity. Step-by-Step Solution: Identify the design goal of humanization: minimize HAMA while preserving binding.Relate preliminary clinical data to this goal: reduced immunogenicity observed.Select the option indicating absence/reduction of HAMA as the principal finding. Verification / Alternative check: Multiple humanized therapeutics (beyond anti-IL-2R) demonstrated decreased anti-drug antibody incidence compared with murine antibodies, supporting the same conclusion. Why Other Options Are Wrong: b: Contradicts the purpose and findings of humanization. c: Patients do recognize human Ig constant regions as self; “poor recognition” is incorrect framing. d/e: Overbroad or false given reduced immunogenicity with humanized constructs. Common Pitfalls: Equating chimeric and humanized antibodies; humanized constructs generally contain less murine sequence than chimeric antibodies and thus even lower immunogenicity. Final Answer: Absence of a significant human immune response against murine proteins (reduced HAMA)

Question 2

Therapeutic monoclonal antibodies (MAbs) — Identify the incorrect statement about clinical uses and disease areas.

Accepted Answer

Introduction / Context: Monoclonal antibodies (MAbs) are versatile biologics used across oncology, autoimmunity, infectious disease, transplantation, and even endocrine-related conditions. The question tests awareness of the breadth of indications and the misconception that MAbs are limited to infections or cancer only. Given Data / Assumptions: MAbs can be conjugated for imaging (tumor scanning) or engineered for therapy (naked, ADCs, radioimmunotherapy). Diagnostic, prognostic, and therapeutic uses span multiple specialties. Endocrine and metabolic disorders can involve MAbs (e.g., anti-PCSK9 for lipid disorders; antibodies targeting IGF-1 receptor pathways in research/therapy). Concept / Approach: Determine which statement artificially restricts MAb utility. Because MAbs are used beyond infectious diseases (e.g., Graves’ ophthalmopathy treatments, metabolic and lipid disorders), any claim that they “cannot be used” in non-infectious endocrine contexts is incorrect. Step-by-Step Solution: Validate positive statements about diagnosis and tumor scanning—these are established uses.Acknowledge extensive oncology diagnostics (immunohistochemistry) and therapeutics.Identify the restrictive statement about endocrine diseases as false. Verification / Alternative check: Approved and investigational antibodies target endocrine axes or metabolic pathways, confirming cross-disciplinary applications. Why Other Options Are Wrong: a/b/c/e: All describe legitimate applications of MAbs in modern medicine. Common Pitfalls: Assuming antibodies are only anti-infective or anti-tumor; in reality, modulation of signaling pathways by MAbs is broadly therapeutic. Final Answer: Monoclonal antibodies cannot be used in non-infectious diseases such as endocrine disorders.

Question 3

Immunology—Helper T lymphocytes (CD4+): In adaptive immunity, helper T cells provide assistance to which cell populations during an immune response?

Accepted Answer

Introduction / Context: Helper T cells (CD4+ T lymphocytes) are central coordinators of the adaptive immune response. Rather than directly killing infected cells, they secrete cytokines and provide costimulatory signals that help other lymphocytes and innate cells perform their effector functions effectively. This question tests understanding of which cell types receive assistance from helper T cells. Given Data / Assumptions: Helper T cells express CD4 and recognize antigen peptides presented on MHC class II molecules. They secrete cytokines and express costimulatory ligands (for example, CD40L) after activation. Target populations for their help include B cells and other T-cell subsets. Concept / Approach: Helper T cells differentiate into functional subsets such as Th1, Th2, Th17, Tfh, and Treg. Th1 cells assist cytotoxic T cells (CD8+) and macrophages via cytokines like IL-2 and IFN-gamma. Tfh cells interact with B cells in germinal centers via CD40L–CD40 and cytokines (for example, IL-21) to drive class switching, affinity maturation, and memory formation. Step-by-Step Solution: Identify the main role of helper T cells → immune coordination via cytokines and costimulation.List recipient cell types → B cells (antibody responses) and other T cells (especially CD8+ priming and expansion).Match with options → assistance extends to both certain B cells and other T cells.Select the option that includes both groups. Verification / Alternative check: Experimental and clinical data show that CD4+ deficiency (for example, untreated HIV infection) impairs antibody class switching and cytotoxic T-cell responses, confirming their dual helper role. Why Other Options Are Wrong: Certain B lymphocytes only: Incomplete; helper T cells also aid CD8+ T cells and macrophages.Certain T lymphocytes only: Incomplete; B-cell help is a hallmark function.None of the above: Contradicts well-established immunology.Only macrophages and neutrophils: Helper T cells do activate macrophages (Th1), but neutrophil control is indirect and B/T help is missing. Common Pitfalls: Confusing CD4+ helper functions with CD8+ cytotoxic functions; thinking helper T cells only influence antibody production while ignoring their role in priming cytotoxic responses. Final Answer: Certain B lymphocytes and other T lymphocytes.

Question 4

B-cell receptor on naive B lymphocytes: Which immunoglobulin is considered the primary surface receptor on mature naive B cells in peripheral lymphoid tissues?

Accepted Answer

Introduction / Context: B cells display membrane-bound immunoglobulin as their antigen receptor (BCR). During development and in the mature naive state, different isotypes can be expressed on the surface. This question probes which isotype is recognized as the primary B-cell receptor on naive B cells circulating in lymphoid organs. Given Data / Assumptions: Naive mature B cells co-express surface IgM and IgD due to alternative RNA splicing of a single heavy-chain transcript. Both isotypes can bind antigen and transduce signals through Ig-alpha/Ig-beta (CD79a/CD79b). Many curricula emphasize IgD as the hallmark BCR on naive mature B cells in secondary lymphoid tissues. Concept / Approach: Although immature B cells initially express IgM, upon maturation they co-express IgM and IgD. In textbooks and exam settings, IgD is often highlighted as the characteristic primary receptor on naive mature B cells in the periphery, while IgM remains present but is more associated with earlier stages and is the first antibody produced upon initial activation. Step-by-Step Solution: Recall developmental sequence: immature B cell → surface IgM; mature naive B cell → surface IgM + IgD.In peripheral lymphoid tissues, IgD is emphasized as the primary BCR marker of naive mature B cells.Select IgD as the best single answer, acknowledging co-expression. Verification / Alternative check: Flow cytometry of mature naive B cells shows strong IgD and IgM; exam conventions typically accept IgD as the defining BCR for naive cells in lymph nodes and spleen. Why Other Options Are Wrong: IgG: Secreted class, mainly after class switching; not the naive BCR.IgA: Mucosal secretions; not primary surface receptor on naive B cells.IgE: Allergy/parasite defense; not surface BCR on naive cells.IgM only: IgM is present, but naive mature B cells co-express IgD; the question seeks the primary hallmark isotype. Common Pitfalls: Ignoring that naive B cells co-express both IgM and IgD; overgeneralizing “first made is IgM” to the identity of the mature naive BCR in lymphoid tissues. Final Answer: IgD (membrane-bound).

Question 5

Monoclonal antibody production: Fusion of antibody-producing mammalian cells with endlessly replicating tumor cells yields what type of cell line?

Accepted Answer

Introduction / Context: The classic hybridoma technology, pioneered by Köhler and Milstein, revolutionized immunology by enabling the production of monoclonal antibodies with a single specificity. Understanding the nature of the fused cell line is essential for biotechnology and diagnostic applications. Given Data / Assumptions: One fusion partner is an antibody-secreting B cell (short-lived). The other is a myeloma cell line (immortal but typically non-secreting and HGPRT-). Successful fusions are selected (for example, in HAT medium) to recover lines that both secrete antibody and proliferate indefinitely. Concept / Approach: Hybridomas inherit immortality from the tumor partner and the antibody gene rearrangements from the B cell. Clonal selection isolates a line producing one antibody specificity in large amounts, underpinning countless assays and therapeutics. Step-by-Step Solution: Recognize fusion outcome → immortal antibody-producing line.Identify correct term → hybridoma.Exclude unfused parental cells or unrelated leukocytes. Verification / Alternative check: Standard protocols show HAT selection rescues HGPRT+ hybrids while eliminating unfused myeloma cells and short-lived B cells. Why Other Options Are Wrong: Myeloma: Tumor partner alone; does not produce the desired antibody.Natural killer cell / Lymphoblast / Plasmablast: Not the fused immortal, monoclonal antibody-secreting line defined by the technique. Common Pitfalls: Confusing the parental myeloma cell line (immortal but non-secreting) with the post-fusion hybridoma that secretes monoclonal antibody. Final Answer: Hybridoma.

Question 6

Cytokine control of lymphocyte expansion: Which cytokine is the principal growth factor that stimulates the activity and proliferation of T cells (and can promote B-cell responses indirectly)?

Accepted Answer

Introduction / Context: Cytokines govern lymphocyte activation, clonal expansion, and differentiation. IL-2 is historically recognized as T-cell growth factor and plays a pivotal role after antigen recognition and costimulation. This question seeks the cytokine best known for directly stimulating T-cell activity and proliferation. Given Data / Assumptions: T cells require signals beyond TCR engagement: costimulation and cytokines. IL-2 is produced mainly by activated CD4+ T cells and acts via the high-affinity IL-2 receptor. B-cell proliferation can be secondarily supported by IL-2-dependent T-cell help and cytokine milieu. Concept / Approach: IL-2 binding to IL-2R (alpha/beta/gamma chains) drives T-cell progression through the cell cycle, survival, and differentiation. While IL-1 is an innate cytokine that enhances T-cell activation, it is not the principal growth factor. Lymphotoxin (TNF-beta) mediates cytotoxicity and lymphoid organ development rather than broad mitogenic stimulation. Step-by-Step Solution: Identify the classic T-cell growth factor → IL-2.Note ancillary roles of IL-1 and TNF-beta but not as primary T-cell mitogens.Select IL-2 as the best single answer. Verification / Alternative check: In vitro T-cell culture requires IL-2; therapeutic IL-2 expands T cells (for example, in adoptive cell therapy). Why Other Options Are Wrong: Lymphotoxin: Cytotoxic cytokine; not the main proliferative signal.IL-1: Costimulatory and pro-inflammatory; not the principal T-cell growth factor.All of these: Over-broad; only IL-2 fits as the canonical growth factor.IL-10: Generally regulatory/anti-inflammatory; suppresses excessive responses. Common Pitfalls: Assuming any pro-inflammatory cytokine drives T-cell proliferation; in classic immunology, IL-2 is the defining T-cell growth factor. Final Answer: Interleukin-2 (IL-2).

Question 7

EBV–hybridoma method: What are the advantages of using the Epstein–Barr virus (EBV) hybridoma technique for generating human monoclonal antibodies?

Accepted Answer

Introduction / Context: Conventional mouse hybridomas are routine, but producing fully human monoclonal antibodies historically required alternative strategies. The EBV-hybridoma approach leverages EBV to transform human B cells, supporting their proliferation and facilitating downstream fusion to create stable antibody-secreting lines. Given Data / Assumptions: EBV infects human B cells and can drive their immortalization. Activated, antigen-experienced B cells proliferate better and are more amenable to fusion. Improved proliferation and survival can increase hybridization success. Concept / Approach: EBV transformation generates lymphoblastoid cell lines that retain antibody gene rearrangements. These lines are expanded and fused with suitable partners to stabilize secretion. The net effect is better availability of antigen-specific clones, higher fusion efficiency, and the ability to derive human monoclonal antibodies without extensive humanization steps. Step-by-Step Solution: Use EBV to immortalize human B cells → sustained growth.Expand antigen-specific pools → enrich desired specificities.Fuse to produce stable, high-yield secreting lines → increased hybridization frequency observed. Verification / Alternative check: Published protocols document EBV transformation followed by selection and fusion, producing human mAbs for diagnostics and research. Why Other Options Are Wrong: Each single option (a–c) is correct but incomplete; the comprehensive advantage is captured by “All of the above.”None of the above: Contradicted by established EBV–B cell biology. Common Pitfalls: Confusing EBV transformation alone with hybridoma creation; EBV helps immortalize and expand B cells, but stable monoclonality still requires fusion and cloning. Final Answer: All of the above.

Question 8

Human monoclonal antibody generation: Which approaches are currently used to obtain human monoclonal antibodies?

Accepted Answer

Introduction / Context: Human monoclonal antibodies can be produced through several laboratory strategies that avoid the immunogenicity issues of mouse antibodies. This question surveys recognized approaches used historically and in many teaching resources for generating fully human monoclonals. Given Data / Assumptions: EBV can transform human B cells to proliferate and secrete antibody. Human plasmacytoma lines can serve as fusion partners for hybridoma formation. Combining EBV transformation (to expand antigen-specific B cells) with fusion increases success. Concept / Approach: EBV-based transformation yields lymphoblastoid lines; fusion with plasmacytoma creates stable hybridomas. Blending methods captures advantages of both: selective expansion of the right B cells and long-term secretion stability. Although modern platforms include transgenic mice and phage display, the options listed reflect classic human cell-derived strategies taught in immunotechnology. Step-by-Step Solution: Recognize each listed approach as a valid route to human mAbs.Note synergy when combining EBV transformation with fusion techniques.Choose the inclusive option encompassing all methods. Verification / Alternative check: Protocols and reviews in immunotechnology literature document these methods as workable paths to human monoclonals. Why Other Options Are Wrong: Single-method answers are incomplete; multiple approaches are valid.None of these is false given the historical context and established techniques. Common Pitfalls: Assuming only one “best” method exists; in practice, labs adopt different pipelines depending on resources and goals. Final Answer: All of these.

Question 9

Immuno-inflammatory disorders (for example, hemolytic anemia, eczema): Which T-cell subset is typically increased in these conditions?

Accepted Answer

Introduction / Context: Immuno-inflammatory disorders often feature dysregulated helper T-cell activity. Conditions such as allergic eczema and certain autoimmune cytopenias are associated with heightened CD4+ T-cell responses and skewed helper subsets (for example, Th2 in atopy), which amplify B-cell activity and inflammatory cascades. Given Data / Assumptions: Disorders mentioned are driven by exaggerated immune activation. CD4+ T cells orchestrate humoral and cellular inflammation through cytokines. In many textbook contexts, these diseases are linked to increased helper T-cell activity. Concept / Approach: Elevated helper function increases cytokine production (for example, IL-4, IL-5, IL-13 in atopy) and provides B-cell help, promoting autoantibody formation in hemolytic anemia. Thus, CD4+ levels and activity are often described as increased in these conditions, aligning with classical MCQ framing. Step-by-Step Solution: Identify the dominant dysregulated arm → helper T cells.Relate helper skewing (Th2) to eczema and autoantibody support in hemolytic anemia.Choose the option indicating increased T4 (CD4+) cells. Verification / Alternative check: Clinical immunology describes elevated helper T-cell activity and cytokine signatures in these diseases; targeted therapies often modulate CD4+ cytokines. Why Other Options Are Wrong: CD8+ increased or decreased: Not the hallmark pattern emphasized in such MCQs.T4 reduced: Opposite of expected dysregulation.No change: Ignores well-known helper T-cell involvement. Common Pitfalls: Equating all inflammatory states with CD8+ cytotoxic dominance; many chronic inflammatory and allergic conditions are CD4+ helper driven. Final Answer: T4 cells (CD4+) are greatly increased.

Question 10

Immortalizing antigen-specific lymphocytes: Which method(s) can be used to render antigen-specific lymphocytes immortal for monoclonal antibody production?

Accepted Answer

Introduction / Context: A key challenge in monoclonal antibody production is that primary antigen-specific lymphocytes are short-lived. Several laboratory strategies confer immortality while preserving antigen specificity, enabling stable antibody secretion and clonal expansion. Given Data / Assumptions: Tumor cell lines provide replicative immortality that can be transferred by fusion or, experimentally, by genetic means. EBV naturally transforms human B cells into proliferating lymphoblastoid cells. Hybridoma formation remains a gold standard for stable monoclonal secretion. Concept / Approach: Immortalization can be achieved by (1) hybridizing antigen-specific lymphocytes with myeloma/plasmacytoma partners, (2) transforming B cells with EBV, and (3) introducing oncogenic or immortalizing elements via tumor-derived DNA. Each approach has trade-offs in stability, efficiency, and safety considerations, but all are recognized in immunotechnology contexts. Step-by-Step Solution: List recognized methods → fusion, EBV transformation, genetic immortalization.Confirm each method enables continuous proliferation.Select the inclusive option. Verification / Alternative check: Historical literature documents successful antibody-secreting lines via EBV, hybridomas, and genetic immortalization strategies. Why Other Options Are Wrong: Any single method alone is incomplete; the question asks for methods (plural) that apply.None of the above contradicts well-established techniques. Common Pitfalls: Assuming hybridoma is the only path; multiple immortalization strategies exist and are taught. Final Answer: All of the above.

Question 11

Cell fusion propensity: When deriving monoclonal antibodies, lymphocytes from lymph nodes or tonsils are especially valuable if their fusion tendencies are at what level?

Accepted Answer

Introduction / Context: Hybridoma formation depends on the efficiency with which primary lymphocytes fuse with immortal partner cells. Tissues rich in activated B cells, such as tonsils or draining lymph nodes after antigen exposure, can yield higher fusion efficiencies, improving chances of obtaining antigen-specific clones. Given Data / Assumptions: Fusion frequency is a limiting factor in hybridoma workflows. Activated, proliferating lymphocytes tend to fuse more readily than resting cells. Higher fusion rates directly translate to more hybridoma candidates. Concept / Approach: When screening for successful fusions in selective media, starting with lymphocytes that exhibit high fusion frequencies maximizes recovery of desired clones. Hence, lymph node or tonsil-derived B cells, often enriched for antigen-experienced cells, are preferred tissue sources. Step-by-Step Solution: Identify the parameter that best predicts hybridoma yield → fusion frequency.Recognize that higher is better for throughput and success.Choose “High frequencies.” Verification / Alternative check: Empirical lab experience shows antigen-stimulated tissues produce more successful fusions than peripheral blood with resting lymphocytes. Why Other Options Are Wrong: Moderate/Low/None: Decrease likelihood of isolating monoclonal lines.Only after repeated freeze–thaw cycles: Damaging; reduces viability and fusion success. Common Pitfalls: Underestimating the importance of starting cell source and activation status on fusion outcomes. Final Answer: High frequencies (fuse readily).

Question 12

Role of cytotoxic T (TC, CD8+) cells: TC cells are most critical for controlling which of the following conditions?

Accepted Answer

Introduction / Context: Cytotoxic T lymphocytes (CTLs; CD8+ T cells) recognize antigenic peptides presented by MHC class I on infected or malignant cells and kill these targets. Their canonical role is the clearance of intracellular pathogens, especially viruses, which rely on host cell machinery to replicate. Given Data / Assumptions: TC cells identify infected cells via TCR recognition of peptide–MHC I complexes. Effector mechanisms include perforin/granzyme pathways and Fas–FasL interactions. Clinical immunodeficiency of CD8+ T cells correlates with susceptibility to persistent viral infections. Concept / Approach: Because viruses replicate inside cells, antibody access is limited; thus, CTL-mediated killing is essential to remove viral reservoirs. Although CTLs may influence some autoimmunity or allergies, they are not the principal drivers there (autoimmunity often involves autoreactive T helper cells and autoantibodies; allergy is mediated by IgE and mast cells). Step-by-Step Solution: Identify the hallmark target of CTLs → virus-infected cells.Contrast with allergy (Th2/IgE/mast cells) and many autoimmune diseases (complex, often CD4+ driven).Select “Virus infections.” Verification / Alternative check: Viral load reductions in acute infections correlate with CTL responses; vaccines that elicit strong CD8+ responses can improve viral control. Why Other Options Are Wrong: Allergy: Dominated by IgE, Th2 cytokines, and mast cells.Autoimmunity: Multifactorial; CTLs may participate but are not the universal primary control mechanism.All of these equally: Overgeneralizes; CTLs are most central for viruses.Helminths only: Helminth defense is typically Th2/eosinophil/IgE dominated. Common Pitfalls: Assuming “strong immunity” always implies cytotoxic T cells; the effector branch depends on pathogen location (intracellular versus extracellular). Final Answer: Virus infections.

Question 13

Immunology basic: identifying the process of antibody-mediated cross-linking What is the term for the cross-linkage of antigens by antibodies, leading to visible clumping or lattice formation?

Accepted Answer

Introduction / Context: In basic immunology, antibodies bind antigens and can physically link multiple antigen particles together. Recognizing the correct term for this antibody-mediated cross-linking is essential for interpreting common serological tests and understanding how immune complexes form in vitro and in vivo. Given Data / Assumptions: Antibodies can bind at least two antigenic determinants (bivalent for IgG; pentameric IgM has high valency). Antigens may be particulate (cells, bacteria, latex beads) or soluble. Question asks specifically about cross-linkage of antigens by antibodies leading to clumping/lattice formation. Concept / Approach: When antibodies bind to antigens on the surface of particles or cells, they can bridge neighboring particles, forming large lattices. This visible clumping is called agglutination. If the antigens are soluble, antibody cross-linking can lead to lattice formation that comes out of solution as a precipitate, termed precipitation. Complement fixation is a different functional assay measuring complement activation, not simply cross-linking. Step-by-Step Solution: Identify the event: antibodies physically link multiple antigen-bearing particles.Recall definitions: agglutination = clumping of cells/particles; precipitation = lattice of soluble antigen and antibody.Match the cross-linkage causing visible clumps with the term agglutination. Verification / Alternative check: Agglutination tests (e.g., ABO blood typing, Widal, latex agglutination) demonstrate antibody-mediated clumping of particulate antigens; this outcome is the classic example of cross-linkage. Why Other Options Are Wrong: Complement fixation: measures whether antibody–antigen complexes fix complement; not simply cross-linkage. Cross-reaction: refers to antibody binding a similar but different antigen; not the physical clumping process. All of these: not correct because only agglutination describes cross-linkage clumping. Precipitation: pertains to soluble antigens forming insoluble lattices, not particulate clumping. Common Pitfalls: Confusing agglutination (particulate) with precipitation (soluble). Always consider whether the antigen is on particles/cells or in solution. Final Answer: Agglutination

Question 14

Monoclonal antibody cross-reactivity: which isotype most often shows unexpected cross-reactions? Identify the monoclonal antibody class that more frequently exhibits unanticipated cross-reactivity in assays due to valency and avidity effects.

Accepted Answer

Introduction / Context: Monoclonal antibodies (MAbs) are prized for specificity, yet cross-reactivity can occur. Understanding which immunoglobulin isotypes are more prone to unexpected reactions helps in assay design, troubleshooting ELISA, agglutination, or immunohistochemistry, and minimizing false positives. Given Data / Assumptions: MAbs can be generated in different isotypes (IgM, IgG, IgA, etc.). IgM exists predominantly as a pentamer in secreted form, offering high valency and avidity. Cross-reactivity may arise from low-affinity interactions stabilized by high avidity. Concept / Approach: IgM antibodies possess 10 potential antigen-binding sites (5 functional pairs), creating very high avidity. Even if each binding site has modest affinity, the overall complex can be stabilized, permitting binding to epitopes of similar shape/charge (heterologous antigens). This increases the likelihood of unexpected cross-reactions relative to monomeric IgG. IgA and IgE are less commonly used in standard diagnostic monoclonals and have different functional roles. Step-by-Step Solution: Consider isotype structure: IgM = pentamer, multivalent; IgG = monomer, bivalent.Higher valency increases apparent binding to related epitopes.Therefore, IgM MAbs more frequently show cross-reactivity in practical assays. Verification / Alternative check: Serological literature and diagnostic kit troubleshooting guides often note that IgM-based reagents may agglutinate nonspecifically or bind related antigens under suboptimal conditions. Why Other Options Are Wrong: IgG MAbs: generally preferred for specificity; lower avidity reduces unintended binding. IgA/Secretory IgA: less commonly used as diagnostic MAbs; not characteristically the main source of cross-reactivity in standard kits. IgE: rare as a monoclonal reagent for routine antigen detection; role is allergic responses. Common Pitfalls: Equating affinity (site-specific strength) with avidity (overall binding strength); IgM can have modest affinity but high avidity, promoting cross-reactions. Final Answer: IgM monoclonal antibodies

Question 15

Antigenicity of small simple molecules — identifying hapten-like behavior Small, structurally simple molecules (without carriers) are generally considered what kind of antigens?

Accepted Answer

Introduction / Context: Immunogenicity depends on size, complexity, and foreignness. Many exam items probe whether students can classify small molecules that cannot, by themselves, elicit strong immune responses. These are often called haptens unless coupled to carriers. Given Data / Assumptions: Molecule is small and chemically simple. No mention of a protein carrier conjugate. Humoral immune response generally targets complex, high-molecular-weight antigens. Concept / Approach: Small simple molecules typically fail to be strongly immunogenic because they lack sufficient epitopic complexity and are poorly processed/presented. When covalently linked to a large carrier protein, they can become immunogenic (hapten–carrier concept). Thus, by themselves, they are poor antigens. Step-by-Step Solution: Assess antigen size and complexity.Recall that haptens require carriers to elicit antibody production.Conclude that such molecules are poor antigens in isolation. Verification / Alternative check: Classic immunology experiments with dinitrophenyl (DNP) and other haptens show no antibody response unless conjugated to a protein carrier like BSA or KLH. Why Other Options Are Wrong: Rich/moderate antigens: contradicts hapten principle. Heterophilic antigens: refer to antigens shared among unrelated species; not about size/complexity. Superantigens: are large microbial proteins that non-specifically activate T cells; opposite of small/simple. Common Pitfalls: Confusing antigenicity (ability to bind) with immunogenicity (ability to elicit a response). Haptens can bind antibodies but usually need carriers to induce them. Final Answer: Poor antigens

Question 16

Sites of lymphocyte maturation in humans — primary lymphoid organs In human immunology, B cells and T cells mature in which primary lymphoid organs, respectively?

Accepted Answer

Introduction / Context: Lymphocyte development occurs in specialized primary lymphoid organs before antigen-driven activation in secondary lymphoid tissues. Correctly identifying maturation sites is foundational for understanding immune ontogeny, immunodeficiencies, and vaccination responses. Given Data / Assumptions: Question pertains to humans (not birds or other species). Focus is maturation (development), not activation. Primary lymphoid organs differ between species. Concept / Approach: In humans, B lymphocytes mature in the bone marrow. T lymphocytes mature in the thymus, where positive and negative selection yield a repertoire that is self-MHC restricted and self-tolerant. Secondary organs (lymph nodes, spleen, MALT) are where mature lymphocytes encounter antigen and undergo activation and clonal expansion. Step-by-Step Solution: Recall species differences: birds use the bursa of Fabricius for B-cell maturation; humans do not have this organ.Identify correct human sites: bone marrow (B cells) and thymus (T cells).Select the option that matches this pairing. Verification / Alternative check: Clinical immunology texts describe severe combined immunodeficiency and DiGeorge syndrome as disorders of marrow-derived lymphopoiesis and thymic development, respectively—underscoring organ-specific roles. Why Other Options Are Wrong: Lymph nodes/spleen: secondary sites; not primary maturation organs. Bursa and thymus: correct for birds, not humans. None/spleen–bone marrow: mismatched or incorrect pairings for human maturation. Common Pitfalls: Transferring avian anatomy (bursa) to humans; conflating maturation with activation sites. Final Answer: Bone marrow and thymus

Question 17

Cytokines made by T lymphocytes — breadth of secreted mediators T cells are a source of which of the following immune mediators?

Accepted Answer

Introduction / Context: T lymphocytes orchestrate immune responses not only through cytotoxicity or help but also via cytokine secretion. Recognizing the variety of mediators produced by T cells clarifies their roles in inflammation, antiviral defense, and B-cell help. Given Data / Assumptions: Activated T cells include Th1, Th2, Th17, Tfh, and cytotoxic subsets. Cytokine profiles are subset-dependent but overlap exists. Lymphotoxin (TNF-beta) is historically linked to activated lymphocytes. Concept / Approach: Helper T cells secrete interleukins such as IL-2, IL-4, IL-17, and others that modulate adaptive responses. T cells (especially Th1 and activated CD8) can produce interferon-gamma, a critical antiviral and macrophage-activating cytokine. Lymphotoxin (TNF-beta) is a T cell–derived member of the TNF family, contributing to lymphoid organogenesis and inflammation. Therefore, T cells are indeed a source of interleukins, interferons (notably IFN-gamma), and lymphotoxin. Step-by-Step Solution: List T cell cytokines: ILs (IL-2, IL-4, etc.), IFN-gamma, and TNF family members.Confirm that each listed class can be produced by activated T cells.Choose the inclusive option. Verification / Alternative check: Standard immunology references detail T cell cytokine profiles; Th1 cells produce IFN-gamma and lymphotoxin; Th2 produce IL-4, IL-5, IL-13; Th17 produce IL-17 family; Tfh produce IL-21. Why Other Options Are Wrong: Single selections (interleukin/interferon/lymphotoxin) are incomplete as T cells can secrete all. Only chemokines: T cells do produce chemokines, but the option excludes the listed cytokines; thus incorrect. Common Pitfalls: Assuming interferons come only from innate cells; IFN-gamma is strongly T cell–derived (and NK-derived). Final Answer: All of these

Question 18

Identifying mosaic antigens — which example best fits? Select the best example of a mosaic antigen, i.e., an antigen displaying multiple distinct epitopes across its surface.

Accepted Answer

Introduction / Context: The term mosaic antigen describes an antigenic structure that presents many different epitopes, allowing multiple antibodies to bind simultaneously. Understanding this concept helps explain strong agglutination, robust neutralization, and polyvalent vaccine strategies. Given Data / Assumptions: Mosaic antigens have complex, repetitive surfaces. Viruses present ordered arrays of proteins on capsids or envelopes. Haptens and small peptides typically offer limited epitopic diversity. Concept / Approach: Viruses, particularly non-enveloped icosahedral viruses, display repeating capsid protein units that create numerous identical and sometimes distinct epitopes across the surface, a classic mosaic organization. Bacteria also have multiple epitopes but are heterogeneous whole organisms; the simplest, clean example used in immunology texts is viral particles. Haptens are too small and simple to qualify, and a single short peptide offers minimal epitope diversity. Step-by-Step Solution: Define mosaic antigen: multiple epitopes in an organized array.Recognize viral capsids/envelopes display multivalent epitopes.Select virus as the best representative example. Verification / Alternative check: Electron micrographs and structural virology demonstrate symmetric arrays of capsid proteins, underpinning polyvalent interactions with antibodies. Why Other Options Are Wrong: Bacterium: complex, but the term mosaic antigen is most classically exemplified by viral capsids. Hapten/small peptide: too simple, not mosaic. Self lipid: generally non-immunogenic and lacks multiple peptide epitopes. Common Pitfalls: Equating organismal complexity (bacteria) with ordered epitope arrays; mosaic refers to the antigenic surface architecture, not organism size. Final Answer: Virus

Question 19

Hybridoma propagation methods — in vitro vs. in vivo How can monoclonal antibody–producing hybrid cells (hybridomas) be propagated for antibody production?

Accepted Answer

Introduction / Context: After fusing antibody-producing B cells with myeloma cells, hybridomas must be expanded to yield monoclonal antibodies. Understanding the two classical production routes informs ethical considerations and scale-up strategies in biotechnology. Given Data / Assumptions: Hybridomas are immortalized antibody-secreting cell lines. Production can be performed in vitro (flasks, bioreactors) or in vivo (ascites). Choice depends on yield, purity, ethics, and regulatory expectations. Concept / Approach: Historically, ascites production in mice yielded high antibody concentrations but raises animal welfare concerns and potential contaminants (host immunoglobulins, proteases). Modern practice favors serum-free in vitro systems, roller bottles, or stirred-tank bioreactors for controlled, scalable, and ethical production. Both approaches are technically valid ways to propagate hybridomas. Step-by-Step Solution: Identify viable propagation routes for hybridomas.Acknowledge that both tissue culture and ascites production are established methods.Select the combined option. Verification / Alternative check: Manufacturing guidelines and lab manuals outline hybridoma culture systems and detail the decline in ascites use in favor of in vitro methods for GMP compliance. Why Other Options Are Wrong: Only in vitro or only in vivo excludes a valid method. None/bioreactor-independent diffusion: inaccurate; practical propagation requires culture systems. Common Pitfalls: Assuming ascites is obsolete; while discouraged, it is still technically possible in some settings. However, expect in vitro systems in modern labs. Final Answer: Both (a) and (b)

Question 20

Species considerations in hybridoma technology — rabbits vs. mice Which statement correctly describes rabbits and mice in the context of myelomas and antibody synthesis used for monoclonal antibody production?

Accepted Answer

Introduction / Context: Classical hybridoma technology relies on fusing antibody-producing B cells with immortal myeloma partners. Species differences have historically shaped which animals are used for monoclonal antibody generation and why mouse systems dominated early monoclonal antibody development. Given Data / Assumptions: Myeloma cell lines are required as fusion partners to confer immortality. Mice have well-established myeloma lines (e.g., SP2/0, NS0). Rabbits are excellent for generating high-affinity antibodies, but classical rabbit myeloma lines were historically lacking. Concept / Approach: Because mice have robust myeloma lines and produce antibodies naturally, they became the standard species for hybridoma production. Rabbits produce antibodies too, but the absence (historically) of stable rabbit myeloma lines limited classic rabbit hybridomas. Modern methods (phage display, transgenic mice, rabbit B-cell immortalization) exist, but the traditional teaching point remains: mouse myelomas are widely available; rabbit myelomas are not. Step-by-Step Solution: Identify species with available myeloma fusion partners: mice.Confirm that mice also synthesize antibodies, enabling hybridoma formation.Conclude the correct statement is that rabbits do not make myelomas whereas mice can synthesize antibodies and have myelomas. Verification / Alternative check: Hybridoma protocols commonly specify mouse myeloma cell lines; rabbit monoclonals typically use alternative technologies rather than classic myeloma fusion. Why Other Options Are Wrong: Claims that mice cannot synthesize antibodies are false. Statements that rabbits make myelomas in the classical sense are historically inaccurate. Equivalence of rabbit and mouse myelomas is incorrect. Common Pitfalls: Confusing antigen production (antibodies) with availability of immortal myeloma fusion partners; the issue is the latter. Final Answer: Rabbits do not make myelomas whereas mice are able to synthesize antibodies

Monoclonal Antibodies Questions